scholarly journals Mutation of the C/EBP binding sites in the Rous sarcoma virus long terminal repeat and gag enhancers.

1993 ◽  
Vol 67 (5) ◽  
pp. 2862-2870 ◽  
Author(s):  
T A Ryden ◽  
M de Mars ◽  
K Beemon
Keyword(s):  
Long Terminal Repeat ◽  
Binding Sites ◽  
Rous Sarcoma Virus ◽  
Terminal Repeat ◽  
Rous Sarcoma ◽  
Sarcoma Virus

Sp1 binding sites inserted into the Rous sarcoma virus long terminal repeat enhance LTR-driven gene expression

Gene ◽  
1998 ◽  
Vol 208 (1) ◽  
pp. 73-82 ◽  
Author(s):  
Ondřej Machoň ◽  
Veronika Strmen ◽  
Jiřı́ Hejnar ◽  
Josef Geryk ◽  
Jan Svoboda
Keyword(s):  
Gene Expression ◽  
Long Terminal Repeat ◽  
Binding Sites ◽  
Rous Sarcoma Virus ◽  
Terminal Repeat ◽  
Rous Sarcoma ◽  
Sarcoma Virus

Identification of transcriptional elements within the long terminal repeat of Rous sarcoma virus

1983 ◽  
Vol 3 (10) ◽  
pp. 1834-1845
Author(s):  
G M Gilmartin ◽  
J T Parsons
Keyword(s):  
Long Terminal Repeat ◽  
Virus Replication ◽  
Rous Sarcoma Virus ◽  
Regulatory Elements ◽  
Terminal Repeat ◽  
Tata Box ◽  
Transcriptional Regulatory Elements ◽  
Rous Sarcoma ◽  
Transcriptional Regulatory ◽  
Sarcoma Virus

Transcriptional regulatory elements within the Rous sarcoma virus long terminal repeat were examined by the construction of a series of deletions and small insertions within the U3 region of the long terminal repeat. The analysis of these mutations in chicken embryo cells and COS cells permitted the identification of important transcriptional regulatory elements. Sequences within the region 31 to 18 base pairs upstream of the RNA cap site (-31 to -18), encompassing a TATA box-like sequence, function in the selection of the correct site of transcription initiation and, in addition, augment the efficiency of transcription. These sequences are essential for virus replication. Sequences within the region -79 to -59, overlapping a CAAT box-like sequence, are not required for virus replication and have no obvious effect on viral RNA transcription in the presence of an intact TATA box. However, in mutants lacking a functional TATA sequence, mutations in this region serve to decrease the efficiency of correct transcriptional initiation events.

Identification of a functional promoter in the long terminal repeat of Rous sarcoma virus

Cell ◽  
1980 ◽  
Vol 22 (3) ◽  
pp. 787-797 ◽  
Author(s):  
Tadashi Yamamoto ◽  
Benoit de Crombrugghe ◽  
Ira Pastan
Keyword(s):  
Long Terminal Repeat ◽  
Rous Sarcoma Virus ◽  
Terminal Repeat ◽  
Rous Sarcoma ◽  
Sarcoma Virus

scholarly journals At least two nuclear proteins bind specifically to the Rous sarcoma virus long terminal repeat enhancer.

1987 ◽  
Vol 7 (2) ◽  
pp. 787-798 ◽  
Author(s):  
L Sealey ◽  
R Chalkley
Keyword(s):  
Long Terminal Repeat ◽  
Rous Sarcoma Virus ◽  
Consensus Sequence ◽  
Simian Virus 40 ◽  
Dnase I ◽  
Terminal Repeat ◽  
Sequence Motifs ◽  
Enhancer Activity ◽  
Rous Sarcoma ◽  
Sarcoma Virus

We used the sensitive gel electrophoresis DNA-binding assay and DNase I footprinting to detect at least two protein factors (EFI and EFII) that bound specifically to the Rous sarcoma virus (RSV) enhancer in vitro. These factors were differentially extracted from quail cell nuclei, recognized different nucleotide sequences in the U3 region of the RSV long terminal repeat, and appeared to bind preferentially to opposite DNA strands as monitored by the DNase I protection assay. The EFI- and EFII-protected regions within U3 corresponded closely to sequences previously demonstrated by deletion mutagenesis to be required for enhancer activity, strongly suggesting a functional significance for these proteins. Only weak homologies between other enhancer consensus sequence motifs and the EFI and EFII recognition sites were observed, and other viral enhancers from simian virus 40 and Moloney murine sarcoma virus did not compete effectively with the RSV enhancer for binding either factor.

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